MSC Neuro 25 p2

Basic Treatment Principles

Correction of respiratory disorders:

Oxygen if saturation <95% (2-4 L/min).

Intubate and ventilate if respiratory rate <12 or >32 per min, hypoxia (pO2 <60 mm Hg), hypercapnia (pCO2 >50 mm Hg), or Glasgow Coma Scale (GCS) <9.

Correction of cardiovascular disorders:

For ischemic stroke (IS), BPallowed up to 220/110 mm Hg during the first 24 hrs (185/110 after thrombolysis).

For hemorrhagic stroke (HS), maintain systolic BP 140-160 mm Hg.

Control arrhythmias, restore rhythm in paroxysmal atrial fibrillation <48 hrs onset with cardiologist.

Intracranial pressure (ICP) management:

Elevate head 30 degrees.

Osmotic diuretics (mannitol 0.5-1 g/kg every 4-6 hrs).

Surgical decompression if indicated (especially in HS).

Glucose control:

Hyperglycemia (>10 mmol/L): IV short-acting insulin.

Hypoglycemia (<2.7 mmol/L): IV glucose 20 ml of 40%.

Water-electrolyte balance:

Moderate positive fluid balance except cerebral edema (negative fluid balance).

Avoid hypotonic fluids (e.g., 5% glucose).

Monitor electrolytes regularly.

Hyperthermia correction:

Cooling, NSAIDs, antihistamines as appropriate.

Nutrition:

Start enteral feeding within 24 hrs if swallowing impaired.

Caloric intake 30 kcal/kg/day.

Prevention and treatment of complications:

DVT& pulmonary embolism: LMWH (enoxaparin 0.4 ml s/c daily) or heparin 5,000 units s/c twice daily.

Aspiration pneumonia: early mobilization, NG tube feeding, antibiotics if needed.

Seizures: benzodiazepines (e.g., diazepam) intravenous as needed.

Oral and eye care regularly.

Specific Treatment

Ischemic Stroke:

Intravenous thrombolysis with alteplase (rtPA) 0.9 mg/kg (max 90 mg) within 4.5 hours of symptom onset.

Intra-arterial thrombolysis or mechanical thrombectomy within 6 hours in eligible patients.

Neuroprotective agents (cerebrolysin, citicoline, actovegin).

Anticholinesterase and cholinergic drugs as adjuncts.

Hemorrhagic Stroke:

Osmotic agents (mannitol).

Sedation with barbiturates or propofol for medical coma if needed.

Surgical decompression when indicated.

8.Chronic cerebral ischemia. Clinic, diagnosis, and treatment. Syndromology features of developmental stages.

Cardioembolic Ischemic Stroke

Etiology / Risk Factors:

Sources of emboli:

Cardiac thrombi (left atrium in atrial fibrillation, left ventricle post-myocardial infarction)

Valvular heart disease vegetations

Aortic and large vessel atherosclerotic plaques

Fat embolism (long bone fractures)

Air embolism (lung surgery, pneumothorax)

Emboli occlude cerebral arteries causing ischemia. Clinical Features:

Sudden onset maximal neurological deficit, often with fluctuating symptoms.

Loss of consciousness and seizures more common than other strokes.

Depending on artery involved:

Middle cerebral artery: unilateral facial weakness, aphasia, dysarthria, monoplegia, sensory aphasia, neglect.

Anterior cerebral artery: sudden contralateral leg weakness.

Posterior cerebral artery: homonymous hemianopia, cortical blindness.

Basilar artery: drowsiness, bilateral cortical blindness.

Posterior Inferior Cerebellar Artery Occlusion (Wallenberg Syndrome)

Clinical Features:

Ipsilateral Horner’s syndrome (ptosis, miosis, enophthalmos)

Ipsilateral facial hypoesthesia

Paresis of soft palate and larynx (dysphagia, dysphonia)

Vertigo, nausea, vomiting, nystagmus

Ipsilateral limb ataxia

Contralateral hemihypesthesia below the neck

Cranial nerve dysfunction and cerebellar signs

Alternating hemiparesis and sensory signs depending on extent

Diagnosis

Brain CT/MRI for localization, type of infarction

Doppler and angiography for vessel status

Echocardiography to identify cardiac embolic source

EEG if seizures present

Blood tests including coagulation, glucose, lipids

Treatment

Hospitalize promptly (within 4–6 hrs if feasible)

Support vital functions, manage blood pressure carefully

Anticoagulation for cardioembolic source (e.g., atrial fibrillation)

Thrombolysis or thrombectomy in eligible ischemic stroke cases

Symptom management: seizures, airway protection, nutrition

Rehabilitation planning for functional recovery

9.Primary and secondary purulent meningitis. Meningococcal infection. Meningococcal meningitis. Etiology, clinic, diagnosis, treatment, forms, treatment, prevention.

Primary Purulent Meningitis

Etiology:

Caused by Gram-negative diplococcus Neisseria meningitidis (Wechselbaum's meningococcus)

Transmitted via respiratory droplets and contact with contaminated objects

Infection enters via mucous membranes of the nasopharynx

Carriers, both healthy and sick, spread infection

Peaks in winter and spring; can be sporadic any time

Pathogenesis:

Purulent inflammation of pia mater and meningeal vessels

Toxic, degenerative, and vascular-inflammatory changes in cerebral cortex

Edema and microabscesses may form

Clinical Features:

Incubation 1-5 days

Acute onset: chills, fever 39-40°C, intense headache, nausea, vomiting

Meningeal signs: neck stiffness, Kernig’s sign

Neurological signs may include convulsions, delirium, impaired consciousness

Cranial nerve involvement (III, VI,VII, VIII) possible

Hemorrhagic skin rashes, herpetic eruptions on lips sometimes present

CSF: turbid, purulent, high pressure, neutrophilic pleocytosis, high protein, low glucose and chlorides

Blood: leukocytosis, elevated ESR

Forms: mild, moderate, and severe

Severe cases may show brain stem involvement with psychomotor agitation, hallucinations, behavioral changes, ataxia, nystagmus

Complications:

Cerebral edema with brainstem involvement, adrenal insufficiency (Waterhouse-Friderichsen syndrome)

Residual neurological deficits: hydrocephalus, dementia, amaurosis (rare)

Treatment:

Prompt hospitalization and antibiotic therapy after CSF sampling

Antibiotics: ampicillin + first-generation cephalosporins in children; penicillin G, ampicillin, or ceftriaxone in adults

Symptomatic management (antipyretics, anticonvulsants, corticosteroids in severe cases)

Supportive care: airway, fluid balance, prevent complications

Close monitoring and hydration

In septic shock, hydrocortisone and supportive infusions administered

Rehabilitation and nootropic drugs post-acute phase for neurological recovery

Prevention:

Isolation of patient and disinfection

Screening and prophylactic treatment of contacts

Vaccination programs in endemic areas

Secondary Purulent Meningitis

Etiology and Pathogenesis:

Caused by direct spread from adjacent infections (otitis, sinusitis), trauma or surgery

Pathogens vary: Group B/D streptococci, E. coli, Listeria monocytogenes, Haemophilus influenzae in children; pneumococci and staphylococci in adults

Clinical Features:

Acute onset with chills, high fever, meningeal syndrome (neck stiffness, Kernig, Brudzinski signs), photophobia

Possible cranial nerve involvement, mental status alterations, convulsions

CSF: purulent with neutrophilic predominance, high protein, low sugar and chlorides

Blood: marked leukocytosis with left shift, elevated ESR

Treatment:

Target underlying infection focus surgical if needed (mastoidectomy in otogenic meningitis)

Empirical broad-spectrum antibiotics started immediately after sampling, later adjusted per culture and sensitivity

Combined systemic and intrathecal antibiotic therapy

Symptomatic management as in primary meningitis

Treatment continued until normal clinical and CSF parameters

Meningococcal infection. Meningococcal meningitis

Etiology

Caused by Neisseria meningitidis (Gram-negative diplococcus, also called Weichselbaum's meningococcus).

Transmission: respiratory droplets and contact with contaminated objects.

Portal of entry: mucous membranes of the nasopharynx.

Humans are the only reservoir; healthy carriers can transmit infection.

Seasonal: more common in winter and spring but can occur year-round.

Clinical Manifestations

Forms:

Localized: meningococcal carriage, acute nasopharyngitis

Generalized: meningococcemia (sepsis), meningitis, meningoencephalitis

Mixed: meningitis + meningococcemia

Rare: endocarditis, pneumonia, iridocyclitis, arthritis

Clinical picture:

Incubation 2-10 days, usually 4 days

Sudden onset with chills, high fever (39-40°C), severe headache

Vomiting (usually without nausea), meningeal signs (neck stiffness, Kernig and Brudzinski signs) appear early and intensify

Psychomotor agitation, delirium, convulsions, altered consciousness may develop

Cranial nerve involvement: III,VI, VII, VIII nerves causing diplopia, ptosis, hearing problems

Hemorrhagic skin rash and herpetic eruptions on lips common, especially in children → signs of meningococcemia

Blood: leukocytosis (up to 16-25 ×10^9 /L), elevated ESR

CSF: purulent, high pressure, neutrophilic pleocytosis, high protein, decreased glucose and chlorine

Severe forms may show brainstem signs, hallucinations, behavioral changes, ataxia, nystagmus

Diagnosis

Clinical examination at presentation.

Lumbar puncture with CSF analysis and Gram staining.

Culture of CSF and blood for meningococcus.

PCR testing to confirm the pathogen.

Differential diagnosis with other etiologies of meningitis and encephalitis.

Course and Forms

Acute fulminant, acute, abortive, and recurrent forms.

Severe forms in children and young adults; mortality increased without treatment.

Complications include cerebral edema, brainstem involvement, WaterhouseFriderichsen syndrome (adrenal hemorrhagic insufficiency).

Treatment

Immediate hospitalization and isolation of the patient till bacteriological clearance.

Early empirical antibiotic therapy after lumbar puncture:

Children: ampicillin + first-generation cephalosporin (cefataxime or ceftriaxone)

Adults: penicillin G, ampicillin, or ceftriaxone

Antipyretics, corticosteroids (for severe cases)

Symptomatic and supportive care: hydration, airway management, anticonvulsants, sedation if required

In septic shock: corticosteroids, fluid resuscitation, vasopressors

Multivitamins and neuroprotective agents post-acute phase

Prevention

Early isolation and disinfection of patient's environment.

Close contacts screened and prophylactically treated.

Medical observation of contacts for 10 days.

Vaccination programs in endemic areas and high-risk groups.

10.Serous meningitis, general characteristics. Tuberculosis and viral meningitis.

1.Serous Meningitis

Etiology:

Mainly caused by viruses such as lymphocytic choriomeningitis virus, Coxsackie, ECHO, polio, measles, mumps, and tubercle bacillus.

Pathology:

Serous inflammation of the pia mater.

Clinical Features:

General symptoms: fever (38–40°C), headache (intense, bursting), dizziness.

Meningeal signs: neck stiffness, Kernig and Brudzinski signs, photophobia.

Neurological: irritation phenomena (epileptic seizures, psychomotor agitation), cranial nerve palsies in severe cases.

Early irritative symptoms due to increased intracranial pressure and meninges stretching.

CSF Findings:

Clear or slightly turbid; lymphocytic pleocytosis (hundreds); elevated protein; normal or slightly reduced glucose.

Treatment:

Symptomatic and supportive, including pain relief, hydration, and sometimes antiviral therapy. Corticosteroids may be used in severe inflammation.

2.Tuberculous Meningitis

Etiology:

Infection with Mycobacterium tuberculosis. Usually secondary to pulmonary or other systemic tuberculosis.

Pathogenesis:

Hematogenous spread of MTB; formation of tubercles in meninges (basal meningitis), inflammation of vessels leading to infarcts.

Clinical Features:

Subacute onset over days to weeks.

Initial signs: headache, malaise, low-grade fever.

Progression: irritability, confusion, vomiting, cranial nerve involvement (III, VI), stiff neck, altered consciousness.

Advanced stages: coma, hemiparesis, dementia, hydrocephalus.

Signs of meningeal irritation more pronounced than in viral meningitis.

CSF Findings:

Elevated opening pressure (up to 500–600 mm H2O).

Clear to slightly turbid fluid with high protein (up to 1–1.5 g/L), lymphocytic pleocytosis.

Significantly reduced glucose and chloride levels.

Acid-fast bacilli may be detected microscopically or via PCR.

Treatment:

Long-term antitubercular therapy including isoniazid, rifampicin, ethambutol, pyrazinamide.

Adjunctive corticosteroids to reduce inflammation.

Prognosis:

Dependent on early diagnosis and therapy; complications include hydrocephalus and neurological deficits.

3.Viral Meningitis

Etiology:

Enteroviruses (Coxsackie, ECHO), mumps, influenza virus, tick-borne encephalitis virus.

Clinical Features:

Often mild course.

Symptoms: fever, headache, photophobia, neck stiffness.

Many cases self-limited.

CSF Findings:

Clear fluid.

Lymphocytic pleocytosis.

Normal glucose and protein.

Treatment:

Supportive: rest, hydration, analgesics for headache and fever. Antivirals in specific infections if indicated.

Avoid fever suppression that may hinder immune response.

Summary and Notes

Diagnosis confirmed via CSF analysis (lumbar puncture), imaging if indicated.

Differential diagnosis critical to exclude hemorrhagic causes and other CNS pathologies.

Early treatment essential to reduce morbidity and mortality in bacterial meningitis.

Vaccination and chemoprophylaxis (e.g., rifampicin) essential in prevention of vaccine-preventable meningitis.

11.Encephalitis: spring-summer tick-borne, herpetic. Etiology, clinic, diagnosis, treatment, prevention.

Tick-borne Encephalitis (TBE): Spring-Summer Tick-borne and Herpetic Encephalitis

Etiology and Transmission: